Bone Marrow p16INK4a-Deficiency Does Not Modulate Obesity, Glucose Homeostasis or Atherosclerosis Development
Figure 5
Bone marrow p16INK4a-deficiency does not alter atherosclerosis development or plaque phenotype.
Ldlr−/− mice transplanted with p16+/+ (p16+/+ BMT ldlr−/−; n = 12) or p16−/− (p16−/− BMT ldlr−/−; n = 12) bone marrow were sacrificed after 9 weeks of western diet. (A) Measurement of lesion surface by Oil Red O staining; (B) lesion profile starting from the aortic root; (C) collagen content was calculated by measuring Sirius red staining intensity relative to plaque size; (D) representative pictures of MCP1 immunostaining; (E) representative pictures of TNF immunostaining. Open circles represent p16+/+ BMT ldlr−/− mice and closed circles represent p16−/− BMT ldlr−/− mice.